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article-17166_19 | Physiology, Acute Phase Reactants -- Pathophysiology | There are some disease states that are causally related to APPs, and some are associated with them. The central role of fibrin during hemostasis and thrombosis is well known. However, fibrinogen also increases the risk of bleeding and thrombosis in many pathologies, including inflammation, infection, neurologic disease, and cancer. CRP can activate complement. In cardiac infarction, CRP has a key role in some forms of tissue alteration. Elevated levels of CRP are associated with the risk of atherosclerosis. [9] | Physiology, Acute Phase Reactants -- Pathophysiology. There are some disease states that are causally related to APPs, and some are associated with them. The central role of fibrin during hemostasis and thrombosis is well known. However, fibrinogen also increases the risk of bleeding and thrombosis in many pathologies, including inflammation, infection, neurologic disease, and cancer. CRP can activate complement. In cardiac infarction, CRP has a key role in some forms of tissue alteration. Elevated levels of CRP are associated with the risk of atherosclerosis. [9] |
article-17166_20 | Physiology, Acute Phase Reactants -- Pathophysiology | The prolonged elevation of serum amyloid A (SAA) can eventually lead to secondary amyloidosis. Amyloidosis is caused by amyloid fibrils (misfolded SAA) depositing extracellularly in various organs, including the heart, liver, tongue, spleen, hematologic, and spleen. Patients can develop symptoms of restrictive cardiomyopathy or arrhythmia, macroglossia, hepatomegaly, splenomegaly, cough, and dyspnea. There is a casual relationship between SAA and amyloid fibrils. However, the cause of misfolded SAA is not fully understood. Sustained high SAA levels, amyloid enhancing factor, apolipoprotein-E4, impaired SAA-degrading proteases, and many other factors have been implicated. Some of the diseased states with a prolonged elevation of SAA include chronic infection, rheumatoid arthritis, familial Mediterranean fever (FMF), inflammatory bowel disease, and malignancy. [10] | Physiology, Acute Phase Reactants -- Pathophysiology. The prolonged elevation of serum amyloid A (SAA) can eventually lead to secondary amyloidosis. Amyloidosis is caused by amyloid fibrils (misfolded SAA) depositing extracellularly in various organs, including the heart, liver, tongue, spleen, hematologic, and spleen. Patients can develop symptoms of restrictive cardiomyopathy or arrhythmia, macroglossia, hepatomegaly, splenomegaly, cough, and dyspnea. There is a casual relationship between SAA and amyloid fibrils. However, the cause of misfolded SAA is not fully understood. Sustained high SAA levels, amyloid enhancing factor, apolipoprotein-E4, impaired SAA-degrading proteases, and many other factors have been implicated. Some of the diseased states with a prolonged elevation of SAA include chronic infection, rheumatoid arthritis, familial Mediterranean fever (FMF), inflammatory bowel disease, and malignancy. [10] |
article-17166_21 | Physiology, Acute Phase Reactants -- Pathophysiology | Alpha-1 antitrypsin (AAT) is released from the liver and acts as a serine protease inhibitor (serpin) that protects the cells from neutrophil elastase activity. AAT deficiency is caused by a mutation in the SERPINA1 gene. The mutation is more common in European descendants. The production of AAT in individuals with the mutation is dependent on the allele type. There are three alleles for the AAT gene: M, S, and Z with autosomal codominant inheritance. The normal allele for the SERPINA1 gene is M, and AAT production in homozygous (PiMM) individuals is normal. The S mutation causes a moderate decrease in AAT production, and the Z mutation causes a significant decrease. Therefore, the severity of the disease is dependent on the genotypic expression. Individuals with two normal alleles, PiMM (protease inhibitor MM), have 100% expression of normal protein and have normal levels of AAT. Individuals with PiMS have 80% of normal serum levels of AAT. Individuals with PiSS, PiMZ, and PiSZ have 40-60% serum levels of AAT. Severe AAT deficiency is in individuals homozygous of the Z allele (PiZZ). They produce 10% of the normal serum AAT. | Physiology, Acute Phase Reactants -- Pathophysiology. Alpha-1 antitrypsin (AAT) is released from the liver and acts as a serine protease inhibitor (serpin) that protects the cells from neutrophil elastase activity. AAT deficiency is caused by a mutation in the SERPINA1 gene. The mutation is more common in European descendants. The production of AAT in individuals with the mutation is dependent on the allele type. There are three alleles for the AAT gene: M, S, and Z with autosomal codominant inheritance. The normal allele for the SERPINA1 gene is M, and AAT production in homozygous (PiMM) individuals is normal. The S mutation causes a moderate decrease in AAT production, and the Z mutation causes a significant decrease. Therefore, the severity of the disease is dependent on the genotypic expression. Individuals with two normal alleles, PiMM (protease inhibitor MM), have 100% expression of normal protein and have normal levels of AAT. Individuals with PiMS have 80% of normal serum levels of AAT. Individuals with PiSS, PiMZ, and PiSZ have 40-60% serum levels of AAT. Severe AAT deficiency is in individuals homozygous of the Z allele (PiZZ). They produce 10% of the normal serum AAT. |
article-17166_22 | Physiology, Acute Phase Reactants -- Pathophysiology | AAT gene mutation induces AAT protein conformation change in the structure. It affects the liver and the lungs. In the liver, AAT accumulates because of impaired secretion. As a result, there is hepatocyte destruction leading to hepatitis and liver cirrhosis. In the lungs, the absence of AAT causes uninhibited neutrophil elastase activity. It leads to the destruction of pulmonary architecture and panacinar emphysema. [1] | Physiology, Acute Phase Reactants -- Pathophysiology. AAT gene mutation induces AAT protein conformation change in the structure. It affects the liver and the lungs. In the liver, AAT accumulates because of impaired secretion. As a result, there is hepatocyte destruction leading to hepatitis and liver cirrhosis. In the lungs, the absence of AAT causes uninhibited neutrophil elastase activity. It leads to the destruction of pulmonary architecture and panacinar emphysema. [1] |
article-17166_23 | Physiology, Acute Phase Reactants -- Clinical Significance | APPs are non-specific markers of inflammation, and the tests used should be interpreted in conjunction with history, physical examination, and other laboratory tests and imaging. Their levels will be elevated during both acute and chronic inflammation. However, the highest levels are attained in acute inflammation during an acute infection or after trauma resulting in CRP of 50 to 100 mg/L and ESR exceeding 50 mm/hour. | Physiology, Acute Phase Reactants -- Clinical Significance. APPs are non-specific markers of inflammation, and the tests used should be interpreted in conjunction with history, physical examination, and other laboratory tests and imaging. Their levels will be elevated during both acute and chronic inflammation. However, the highest levels are attained in acute inflammation during an acute infection or after trauma resulting in CRP of 50 to 100 mg/L and ESR exceeding 50 mm/hour. |
article-17166_24 | Physiology, Acute Phase Reactants -- Clinical Significance | The best recent evidence relates to procalcitonin (PCT). PCT levels can be used to guide treatment in patients with pneumonia. PCT levels greater than 0.25 mcg/L correlate with bacterial infections of the lower respiratory tract. After 2 or 3 days of treatment, lower PCT levels can facilitate the decision to discontinue pneumonia antibiotic treatment. PCT levels greater than 0.5 ng/mL can confirm sepsis. PCT should not be used for the diagnosis of pneumonia or for deciding if the antibiotics are necessary to treat pneumonia. It should only be as a guide antibiotic treatment. [11] | Physiology, Acute Phase Reactants -- Clinical Significance. The best recent evidence relates to procalcitonin (PCT). PCT levels can be used to guide treatment in patients with pneumonia. PCT levels greater than 0.25 mcg/L correlate with bacterial infections of the lower respiratory tract. After 2 or 3 days of treatment, lower PCT levels can facilitate the decision to discontinue pneumonia antibiotic treatment. PCT levels greater than 0.5 ng/mL can confirm sepsis. PCT should not be used for the diagnosis of pneumonia or for deciding if the antibiotics are necessary to treat pneumonia. It should only be as a guide antibiotic treatment. [11] |
article-17166_25 | Physiology, Acute Phase Reactants -- Clinical Significance | The normal ESR value for men is 0 to 15 mm/hour and for women 0 to 20 mm/hour. Factors that increase ESR include infection, inflammation, malignancy, pregnancy, autoimmune diseases (SLE, RA, GCA, polymyalgia rheumatic, thyroiditis), multiple myeloma, Waldenstrom macroglobulinemia, anemia, macrocytosis, and old age. Factors that decrease ESR include hypogammaglobulinemia, hypofibrinogenemia, microcytosis, spherocytosis, sickle cell disease, polycythemia, and extreme leukocytosis (e.g., chronic lymphocytic leukemia). | Physiology, Acute Phase Reactants -- Clinical Significance. The normal ESR value for men is 0 to 15 mm/hour and for women 0 to 20 mm/hour. Factors that increase ESR include infection, inflammation, malignancy, pregnancy, autoimmune diseases (SLE, RA, GCA, polymyalgia rheumatic, thyroiditis), multiple myeloma, Waldenstrom macroglobulinemia, anemia, macrocytosis, and old age. Factors that decrease ESR include hypogammaglobulinemia, hypofibrinogenemia, microcytosis, spherocytosis, sickle cell disease, polycythemia, and extreme leukocytosis (e.g., chronic lymphocytic leukemia). |
article-17166_26 | Physiology, Acute Phase Reactants -- Clinical Significance | Some of the APRs, like CRP, are unique because they can be used in cardiovascular risk assessment for patients. It has also been shown in patients with acute coronary syndromes that elevated CRP levels assayed by the high sensitivity (hsCRP) assay are indicative of poor cardiovascular prognosis. Poor prognosis includes increased mortality, post-myocardial infarction, and unstable angina, among others. In patients without ASCVD, a hsCRP between 3 to 20 mg/L, on two occasions at least six weeks apart, confers an increased risk for ASCVD provided a nidus for inflammation has been excluded. [12] | Physiology, Acute Phase Reactants -- Clinical Significance. Some of the APRs, like CRP, are unique because they can be used in cardiovascular risk assessment for patients. It has also been shown in patients with acute coronary syndromes that elevated CRP levels assayed by the high sensitivity (hsCRP) assay are indicative of poor cardiovascular prognosis. Poor prognosis includes increased mortality, post-myocardial infarction, and unstable angina, among others. In patients without ASCVD, a hsCRP between 3 to 20 mg/L, on two occasions at least six weeks apart, confers an increased risk for ASCVD provided a nidus for inflammation has been excluded. [12] |
article-17166_27 | Physiology, Acute Phase Reactants -- Clinical Significance | CRP is a highly sensitive marker for detecting inflammation. It is not specific to any disease or organ and has a half-life of 24 hours. In patients with systemic lupus erythematosus (SLE), CRP is often within normal limits, and ESR is generally elevated. In SLE patients with elevated high-sensitivity CRP (hsCRP), an infection should be ruled out because elevated hsCRP is a predictor for active infection with high specificity in patients with SLE. [13] | Physiology, Acute Phase Reactants -- Clinical Significance. CRP is a highly sensitive marker for detecting inflammation. It is not specific to any disease or organ and has a half-life of 24 hours. In patients with systemic lupus erythematosus (SLE), CRP is often within normal limits, and ESR is generally elevated. In SLE patients with elevated high-sensitivity CRP (hsCRP), an infection should be ruled out because elevated hsCRP is a predictor for active infection with high specificity in patients with SLE. [13] |
article-17166_28 | Physiology, Acute Phase Reactants -- Clinical Significance | The cell-mediated response to endothelial injury causes giant-cell arteritis (GCA). It involves monocytes differentiating into giant cells and macrophages within the vessel walls producing IL-6. As mentioned above, IL-6 is an AP protein that mediates the systemic response to inflammation like fever, weight loss and causes the liver to produce other acute-phase proteins. It is also responsible for elevated ESR in patients with GCA. Tocilizumab is an IL-6 receptor inhibitor used in patients with GCA, and it can reduce relapses and lower glucocorticoid requirements to maintain disease remission. [14] | Physiology, Acute Phase Reactants -- Clinical Significance. The cell-mediated response to endothelial injury causes giant-cell arteritis (GCA). It involves monocytes differentiating into giant cells and macrophages within the vessel walls producing IL-6. As mentioned above, IL-6 is an AP protein that mediates the systemic response to inflammation like fever, weight loss and causes the liver to produce other acute-phase proteins. It is also responsible for elevated ESR in patients with GCA. Tocilizumab is an IL-6 receptor inhibitor used in patients with GCA, and it can reduce relapses and lower glucocorticoid requirements to maintain disease remission. [14] |
article-17166_29 | Physiology, Acute Phase Reactants -- Review Questions | Access free multiple choice questions on this topic. Comment on this article. | Physiology, Acute Phase Reactants -- Review Questions. Access free multiple choice questions on this topic. Comment on this article. |
article-31526_0 | Scleroderma and Renal Crisis -- Continuing Education Activity | Scleroderma renal crisis is a life-threatening complication of scleroderma. It typically presents with the abrupt onset of severe hypertension accompanied by rapidly progressive renal failure, hypertensive encephalopathy, congestive heart failure, and/or microangiopathic hemolytic anemia. This activity describes the evaluation, diagnosis, and management of scleroderma renal crisis and stresses the role of team-based interprofessional care for affected patients. | Scleroderma and Renal Crisis -- Continuing Education Activity. Scleroderma renal crisis is a life-threatening complication of scleroderma. It typically presents with the abrupt onset of severe hypertension accompanied by rapidly progressive renal failure, hypertensive encephalopathy, congestive heart failure, and/or microangiopathic hemolytic anemia. This activity describes the evaluation, diagnosis, and management of scleroderma renal crisis and stresses the role of team-based interprofessional care for affected patients. |
article-31526_1 | Scleroderma and Renal Crisis -- Continuing Education Activity | Objectives: Describe factors that suggest increased risk of developing scleroderma renal crisis. Review the typical presentation of scleroderma renal crisis. Explain the management of scleroderma renal crisis. Identify strategies to optimize care coordination among interprofessional team members to improve outcomes for patients affected by scleroderma renal crisis. Access free multiple choice questions on this topic. | Scleroderma and Renal Crisis -- Continuing Education Activity. Objectives: Describe factors that suggest increased risk of developing scleroderma renal crisis. Review the typical presentation of scleroderma renal crisis. Explain the management of scleroderma renal crisis. Identify strategies to optimize care coordination among interprofessional team members to improve outcomes for patients affected by scleroderma renal crisis. Access free multiple choice questions on this topic. |
article-31526_2 | Scleroderma and Renal Crisis -- Introduction | Scleroderma renal crisis is a life-threatening complication of scleroderma and presents with the abrupt onset of severe hypertension accompanied by rapidly progressive renal failure, hypertensive encephalopathy, congestive heart failure, and/or microangiopathic hemolytic anemia. | Scleroderma and Renal Crisis -- Introduction. Scleroderma renal crisis is a life-threatening complication of scleroderma and presents with the abrupt onset of severe hypertension accompanied by rapidly progressive renal failure, hypertensive encephalopathy, congestive heart failure, and/or microangiopathic hemolytic anemia. |
article-31526_3 | Scleroderma and Renal Crisis -- Etiology | Most cases of scleroderma renal crisis occur in patients with diffuse scleroderma (10% to 25%) as compared to only 1% to 2% of patients with limited disease. The disease usually occurs early in the course of scleroderma, up to 75% of cases of scleroderma renal crisis developing within the first 4 years from the diagnosis with the median duration of scleroderma at the time of diagnosis of scleroderma renal crisis being 8 months. It may sometimes be the initial presenting feature of scleroderma (scleroderma renal crisis sans scleroderma). | Scleroderma and Renal Crisis -- Etiology. Most cases of scleroderma renal crisis occur in patients with diffuse scleroderma (10% to 25%) as compared to only 1% to 2% of patients with limited disease. The disease usually occurs early in the course of scleroderma, up to 75% of cases of scleroderma renal crisis developing within the first 4 years from the diagnosis with the median duration of scleroderma at the time of diagnosis of scleroderma renal crisis being 8 months. It may sometimes be the initial presenting feature of scleroderma (scleroderma renal crisis sans scleroderma). |
article-31526_4 | Scleroderma and Renal Crisis -- Etiology | Factors predictive of scleroderma renal crisis include diffuse skin involvement, especially with rapid progression, the presence of anti-RNA polymerase III antibodies, corticosteroid therapy in doses greater than 15 mg a day, tendon friction rubs, new onset anemia, pericarditis, and congestive heart failure. [1] [2] [3] [4] [5] | Scleroderma and Renal Crisis -- Etiology. Factors predictive of scleroderma renal crisis include diffuse skin involvement, especially with rapid progression, the presence of anti-RNA polymerase III antibodies, corticosteroid therapy in doses greater than 15 mg a day, tendon friction rubs, new onset anemia, pericarditis, and congestive heart failure. [1] [2] [3] [4] [5] |
article-31526_5 | Scleroderma and Renal Crisis -- Epidemiology | Scleroderma renal crisis was reported to occur in as many as 20% of patients with scleroderma in the older literature, but the prevalence of this disease seems to be decreasing and currently reported to occur in about 5- 10 % of patients with scleroderma. Early studies suggested that African-American patients and males were more likely to develop scleroderma renal crisis but later studies have not born this out. The prevalence rate also is different in different countries, and there is a seasonal variation in presentation with a greater number of patients presenting in winter and fall months. | Scleroderma and Renal Crisis -- Epidemiology. Scleroderma renal crisis was reported to occur in as many as 20% of patients with scleroderma in the older literature, but the prevalence of this disease seems to be decreasing and currently reported to occur in about 5- 10 % of patients with scleroderma. Early studies suggested that African-American patients and males were more likely to develop scleroderma renal crisis but later studies have not born this out. The prevalence rate also is different in different countries, and there is a seasonal variation in presentation with a greater number of patients presenting in winter and fall months. |
article-31526_6 | Scleroderma and Renal Crisis -- Pathophysiology | The pathogenesis of scleroderma renal crisis is not well understood. Injury to the endothelial cells results in structural changes in the blood vessels (intimal thickening and proliferation, fibrin deposition) in the initial stages. Decreased blood flow from the structural changes in the blood vessels as well as renal vasospasm (“Raynaud’s phenomenon”) causes renal ischemia, hyperplasia of the juxtaglomerular apparatus, activation of the renin-angiotensin-aldosterone system (RAAS), and rise in BP. The critical rise in BP causes further damage to renal blood vessels and initiates a vicious cycle eventually leading to malignant hypertension. [1] | Scleroderma and Renal Crisis -- Pathophysiology. The pathogenesis of scleroderma renal crisis is not well understood. Injury to the endothelial cells results in structural changes in the blood vessels (intimal thickening and proliferation, fibrin deposition) in the initial stages. Decreased blood flow from the structural changes in the blood vessels as well as renal vasospasm (“Raynaud’s phenomenon”) causes renal ischemia, hyperplasia of the juxtaglomerular apparatus, activation of the renin-angiotensin-aldosterone system (RAAS), and rise in BP. The critical rise in BP causes further damage to renal blood vessels and initiates a vicious cycle eventually leading to malignant hypertension. [1] |
article-31526_7 | Scleroderma and Renal Crisis -- Histopathology | Changes are seen characteristically in small interlobular and arcuate arteries, and the predominant pathologic changes are similar to those observed in malignant hypertension and other thrombotic microangiopathies. [1] [2] [6] [7] [8] | Scleroderma and Renal Crisis -- Histopathology. Changes are seen characteristically in small interlobular and arcuate arteries, and the predominant pathologic changes are similar to those observed in malignant hypertension and other thrombotic microangiopathies. [1] [2] [6] [7] [8] |
article-31526_8 | Scleroderma and Renal Crisis -- Histopathology | Myxoid intimal proliferation with luminal narrowing occurs early and as the lesions progress, smooth muscle cell infiltration and deposition of collagen occurs in the intima, resulting in the appearance of concentric fibrosis or “onion skin” appearance. Superimposed fibrin thrombi and fibrinoid necrosis of the media are also seen. [1] [2] [6] [7] | Scleroderma and Renal Crisis -- Histopathology. Myxoid intimal proliferation with luminal narrowing occurs early and as the lesions progress, smooth muscle cell infiltration and deposition of collagen occurs in the intima, resulting in the appearance of concentric fibrosis or “onion skin” appearance. Superimposed fibrin thrombi and fibrinoid necrosis of the media are also seen. [1] [2] [6] [7] |
article-31526_9 | Scleroderma and Renal Crisis -- Histopathology | Glomeruli may show ischemic collapse or fibrinoid necrosis. The tubules show changes due to ischemic injury with tubular degeneration and necrosis in acute stages. In the chronic stages, tubular atrophy and interstitial fibrosis develop and are proportional to vascular injury. [7] | Scleroderma and Renal Crisis -- Histopathology. Glomeruli may show ischemic collapse or fibrinoid necrosis. The tubules show changes due to ischemic injury with tubular degeneration and necrosis in acute stages. In the chronic stages, tubular atrophy and interstitial fibrosis develop and are proportional to vascular injury. [7] |
article-31526_10 | Scleroderma and Renal Crisis -- History and Physical | The typical presentation of scleroderma renal crisis is a combination of abrupt onset of severe hypertension associated with oligo-anuric acute renal failure in a patient with diffuse scleroderma. Non-nephrotic proteinuria and hematuria with benign urine sediment are common. Other clinical features include hypertensive retinopathy, encephalopathy with a headache, confusion, change in mental status and altered vision, congestive heart failure, thrombocytopenia, and microangiopathic hemolytic anemia.[ [1] [2] . | Scleroderma and Renal Crisis -- History and Physical. The typical presentation of scleroderma renal crisis is a combination of abrupt onset of severe hypertension associated with oligo-anuric acute renal failure in a patient with diffuse scleroderma. Non-nephrotic proteinuria and hematuria with benign urine sediment are common. Other clinical features include hypertensive retinopathy, encephalopathy with a headache, confusion, change in mental status and altered vision, congestive heart failure, thrombocytopenia, and microangiopathic hemolytic anemia.[ [1] [2] . |
article-31526_11 | Scleroderma and Renal Crisis -- Evaluation | Renal biopsy is not necessary in a classic setting but may be needed in patients with an atypical presentation, for example, a patient with scleroderma with rising serum creatinine who is normotensive or has either active urine sediment or nephrotic range proteinuria. [7] | Scleroderma and Renal Crisis -- Evaluation. Renal biopsy is not necessary in a classic setting but may be needed in patients with an atypical presentation, for example, a patient with scleroderma with rising serum creatinine who is normotensive or has either active urine sediment or nephrotic range proteinuria. [7] |
article-31526_12 | Scleroderma and Renal Crisis -- Treatment / Management | Activation of RAAS plays a crucial role in the pathogenesis of scleroderma renal crisis. Furthermore, the use of angiotensin-converting enzyme inhibitors (ACEIs) in this condition has dropped 1-year mortality to 24% from 85% before the use of these drugs. Therefore, the current practice is to lower blood pressure rapidly with ACEIs and maintain it. [1] [3] [9] | Scleroderma and Renal Crisis -- Treatment / Management. Activation of RAAS plays a crucial role in the pathogenesis of scleroderma renal crisis. Furthermore, the use of angiotensin-converting enzyme inhibitors (ACEIs) in this condition has dropped 1-year mortality to 24% from 85% before the use of these drugs. Therefore, the current practice is to lower blood pressure rapidly with ACEIs and maintain it. [1] [3] [9] |
article-31526_13 | Scleroderma and Renal Crisis -- Treatment / Management | Once the diagnosis of scleroderma renal crisis is made, the patient should be hospitalized, and ACEI therapy started. It is usual, to begin with, short-acting ACEI like captopril and rapidly titrate the dose to lower systolic blood pressure (BP) by about 20 mm Hg in 24 hours and reaching goal BP of 120/70 mm Hg within 72 hours while avoiding hypotension. Once BP is at goal and dose stabilized, long-acting ACEI can be substituted in equivalent doses. | Scleroderma and Renal Crisis -- Treatment / Management. Once the diagnosis of scleroderma renal crisis is made, the patient should be hospitalized, and ACEI therapy started. It is usual, to begin with, short-acting ACEI like captopril and rapidly titrate the dose to lower systolic blood pressure (BP) by about 20 mm Hg in 24 hours and reaching goal BP of 120/70 mm Hg within 72 hours while avoiding hypotension. Once BP is at goal and dose stabilized, long-acting ACEI can be substituted in equivalent doses. |
article-31526_14 | Scleroderma and Renal Crisis -- Treatment / Management | If BP cannot be controlled with maximum doses of ACEI, a dihydropyridine calcium channel blocker can be added. Diuretics should be avoided (unless dictated by the need to control volume status) because they may further stimulate RAAS. | Scleroderma and Renal Crisis -- Treatment / Management. If BP cannot be controlled with maximum doses of ACEI, a dihydropyridine calcium channel blocker can be added. Diuretics should be avoided (unless dictated by the need to control volume status) because they may further stimulate RAAS. |
article-31526_15 | Scleroderma and Renal Crisis -- Treatment / Management | ACEI therapy may result in further decline in function to the point of necessity to initiate dialysis therapy. Continued therapy is recommended as approximately 50% of these patients may recover sufficient kidney function over 3 to 18 months to discontinue dialysis. | Scleroderma and Renal Crisis -- Treatment / Management. ACEI therapy may result in further decline in function to the point of necessity to initiate dialysis therapy. Continued therapy is recommended as approximately 50% of these patients may recover sufficient kidney function over 3 to 18 months to discontinue dialysis. |
article-31526_16 | Scleroderma and Renal Crisis -- Treatment / Management | Even though the use of these ACEIs has resulted in improvement in outcome of patients with scleroderma renal crisis, they do not prevent the disease and may increase the risk of death if used before the development of scleroderma renal crisis. This may be due to delay in making a diagnosis of this disease due to normalization of BP. | Scleroderma and Renal Crisis -- Treatment / Management. Even though the use of these ACEIs has resulted in improvement in outcome of patients with scleroderma renal crisis, they do not prevent the disease and may increase the risk of death if used before the development of scleroderma renal crisis. This may be due to delay in making a diagnosis of this disease due to normalization of BP. |
article-31526_17 | Scleroderma and Renal Crisis -- Treatment / Management | Elevated circulating endothelin-1 have been described in scleroderma and endothelin receptor antagonists may have a role in the management of scleroderma renal crisis. A vasodilating prostaglandin (prostacyclin) may provide both rapid control of blood pressure and improved renal blood flow. Renal recovery may occur as long as 24 months after development of scleroderma renal crisis, and decisions about renal transplantation should be postponed until that time. | Scleroderma and Renal Crisis -- Treatment / Management. Elevated circulating endothelin-1 have been described in scleroderma and endothelin receptor antagonists may have a role in the management of scleroderma renal crisis. A vasodilating prostaglandin (prostacyclin) may provide both rapid control of blood pressure and improved renal blood flow. Renal recovery may occur as long as 24 months after development of scleroderma renal crisis, and decisions about renal transplantation should be postponed until that time. |
article-31526_18 | Scleroderma and Renal Crisis -- Treatment / Management | There is significant survival benefit of successful renal transplantation compared with long-term dialysis. Renal transplant recipients, however, have lower graft survival rates compared to non-scleroderma patients and patient survival rates are lower as well, most likely due to the progression of disease in other visceral organs. Recurrence of scleroderma renal crisis in the transplanted kidney is uncommon (5%) but has been described, particularly in patients who had a more aggressive disease before transplantation. [2] [3] . | Scleroderma and Renal Crisis -- Treatment / Management. There is significant survival benefit of successful renal transplantation compared with long-term dialysis. Renal transplant recipients, however, have lower graft survival rates compared to non-scleroderma patients and patient survival rates are lower as well, most likely due to the progression of disease in other visceral organs. Recurrence of scleroderma renal crisis in the transplanted kidney is uncommon (5%) but has been described, particularly in patients who had a more aggressive disease before transplantation. [2] [3] . |
article-31526_19 | Scleroderma and Renal Crisis -- Differential Diagnosis | Thrombotic microangiopathy, malignant hypertension, and rapidly progressive glomerulonephritis frequently enter into the differential diagnosis of scleroderma renal crisis. | Scleroderma and Renal Crisis -- Differential Diagnosis. Thrombotic microangiopathy, malignant hypertension, and rapidly progressive glomerulonephritis frequently enter into the differential diagnosis of scleroderma renal crisis. |
article-31526_20 | Scleroderma and Renal Crisis -- Differential Diagnosis | BP is markedly elevated in both malignant hypertension and scleroderma renal crisis, and it may be difficult to distinguish between the two unless there is a clear-cut history of antecedent poorly controlled hypertension. | Scleroderma and Renal Crisis -- Differential Diagnosis. BP is markedly elevated in both malignant hypertension and scleroderma renal crisis, and it may be difficult to distinguish between the two unless there is a clear-cut history of antecedent poorly controlled hypertension. |
article-31526_21 | Scleroderma and Renal Crisis -- Differential Diagnosis | In rapidly progressive glomerulonephritis, blood pressure is mildly elevated, urine sediment is nephritic, and there is a greater degree of proteinuria compared to scleroderma renal crisis. In cases that are not clear, serological testing for various causes of rapidly progressive glomerulonephritis would be indicated. In patients who develop scleroderma renal crisis as the initial manifestation of scleroderma, renal biopsy may be the only way to clinch the diagnosis. | Scleroderma and Renal Crisis -- Differential Diagnosis. In rapidly progressive glomerulonephritis, blood pressure is mildly elevated, urine sediment is nephritic, and there is a greater degree of proteinuria compared to scleroderma renal crisis. In cases that are not clear, serological testing for various causes of rapidly progressive glomerulonephritis would be indicated. In patients who develop scleroderma renal crisis as the initial manifestation of scleroderma, renal biopsy may be the only way to clinch the diagnosis. |
article-31526_22 | Scleroderma and Renal Crisis -- Prognosis | ACEIs have changed the outcome of patients with scleroderma renal crisis. Before the use of these drugs, a 1-year survival rate of patients with this disease did not exceed 10%; whereas, patients treated with ACE inhibitors now can anticipate 85% survival at 1 year and 65% survival at 5 years. [10] | Scleroderma and Renal Crisis -- Prognosis. ACEIs have changed the outcome of patients with scleroderma renal crisis. Before the use of these drugs, a 1-year survival rate of patients with this disease did not exceed 10%; whereas, patients treated with ACE inhibitors now can anticipate 85% survival at 1 year and 65% survival at 5 years. [10] |
article-31526_23 | Scleroderma and Renal Crisis -- Prognosis | Up to two-thirds of patients with scleroderma renal crisis may require renal replacement therapy. Half of these patients will eventually recover sufficient renal function to discontinue dialysis. Dialysis status affects the mortality rate in scleroderma renal crisis, mortality being greater in dialyzed patients versus those who do not need dialysis, and being lesser in those whose renal function improved and were able to come off dialysis versus those who needed to continue dialysis. Risk factors for poor outcome in scleroderma renal crisis include the following [1] : Serum creatinine greater than 3 mg/dl at presentation Delay in initiating antihypertensive treatment Inadequate BP control Older age Male gender Congestive heart failure Scleroderma renal crisis occurring without hypertension Renal biopsy findings showing arteriolar fibrinoid necrosis, severe glomerular ischemic collapse or severe tubular atrophy and interstitial fibrosis | Scleroderma and Renal Crisis -- Prognosis. Up to two-thirds of patients with scleroderma renal crisis may require renal replacement therapy. Half of these patients will eventually recover sufficient renal function to discontinue dialysis. Dialysis status affects the mortality rate in scleroderma renal crisis, mortality being greater in dialyzed patients versus those who do not need dialysis, and being lesser in those whose renal function improved and were able to come off dialysis versus those who needed to continue dialysis. Risk factors for poor outcome in scleroderma renal crisis include the following [1] : Serum creatinine greater than 3 mg/dl at presentation Delay in initiating antihypertensive treatment Inadequate BP control Older age Male gender Congestive heart failure Scleroderma renal crisis occurring without hypertension Renal biopsy findings showing arteriolar fibrinoid necrosis, severe glomerular ischemic collapse or severe tubular atrophy and interstitial fibrosis |
article-31526_24 | Scleroderma and Renal Crisis -- Pearls and Other Issues | Scleroderma renal crisis presents with the abrupt onset of severe hypertension accompanied by rapidly progressive renal failure, hypertensive encephalopathy, congestive heart failure, and/or microangiopathic hemolytic anemia. RAAS activation plays a crucial role in the pathogenesis of scleroderma renal crisis, and use of angiotensin-converting enzyme inhibitors (ACEIs) 1-year mortality which was 85% before the use of these drugs has dropped to 24% with the use of these drugs. Therefore, the current practice is to lower blood pressure rapidly with ACEIs and maintain it. | Scleroderma and Renal Crisis -- Pearls and Other Issues. Scleroderma renal crisis presents with the abrupt onset of severe hypertension accompanied by rapidly progressive renal failure, hypertensive encephalopathy, congestive heart failure, and/or microangiopathic hemolytic anemia. RAAS activation plays a crucial role in the pathogenesis of scleroderma renal crisis, and use of angiotensin-converting enzyme inhibitors (ACEIs) 1-year mortality which was 85% before the use of these drugs has dropped to 24% with the use of these drugs. Therefore, the current practice is to lower blood pressure rapidly with ACEIs and maintain it. |
article-31526_25 | Scleroderma and Renal Crisis -- Enhancing Healthcare Team Outcomes | Scleroderma renal crisis is a serious complication of scleroderma and requires close coordination of care between patient's primary care physician, rheumatologist and nephrologist. Early diagnosis and prompt initiation of treatment with ACEis is essential for better outcomes and despite transient worsening of renal function and rise of serum creatinine, continued therapy with ACEI is warranted and may potentially lead to eventual recovery of renal function. [9] [10] | Scleroderma and Renal Crisis -- Enhancing Healthcare Team Outcomes. Scleroderma renal crisis is a serious complication of scleroderma and requires close coordination of care between patient's primary care physician, rheumatologist and nephrologist. Early diagnosis and prompt initiation of treatment with ACEis is essential for better outcomes and despite transient worsening of renal function and rise of serum creatinine, continued therapy with ACEI is warranted and may potentially lead to eventual recovery of renal function. [9] [10] |
article-31526_26 | Scleroderma and Renal Crisis -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | Scleroderma and Renal Crisis -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-51306_0 | Catheter Management of Atrial Septal Defect -- Continuing Education Activity | Transcatheter closure of the ASD is currently available for secundum type of ASDs, and currently, there are two FDA-approved devices in the United States for the closure of ASD. This activity reviews the technique of ASD closure, indications, contraindications and highlights the interprofessional team's role in managing patients with congenital heart defects. | Catheter Management of Atrial Septal Defect -- Continuing Education Activity. Transcatheter closure of the ASD is currently available for secundum type of ASDs, and currently, there are two FDA-approved devices in the United States for the closure of ASD. This activity reviews the technique of ASD closure, indications, contraindications and highlights the interprofessional team's role in managing patients with congenital heart defects. |
article-51306_1 | Catheter Management of Atrial Septal Defect -- Continuing Education Activity | Objectives: Identify the technique of catheter management of ASD. Describe the indications for catheter management of ASD. Recall the complications of catheter management of ASD. To improve outcomes, discuss the importance of interprofessional team care when managing patients undergoing ASD closure with a catheter. Access free multiple choice questions on this topic. | Catheter Management of Atrial Septal Defect -- Continuing Education Activity. Objectives: Identify the technique of catheter management of ASD. Describe the indications for catheter management of ASD. Recall the complications of catheter management of ASD. To improve outcomes, discuss the importance of interprofessional team care when managing patients undergoing ASD closure with a catheter. Access free multiple choice questions on this topic. |
article-51306_2 | Catheter Management of Atrial Septal Defect -- Introduction | Atrial septal defect (ASD) is one of the most common congenital heart defects with an estimated incidence of 6 to 10 per 10,000 live births. [1] Atrial septal defects are classified as primum, secundum, sinus venosus, and coronary sinus defects. The onset of symptoms varies among different patients, and many patients remain asymptomatic. Larger defects tend to cause symptoms early on, and smaller defects cause symptoms later in life. Symptoms include failure to thrive, shortness of breath, palpitations, enlargement of right heart chambers, peripheral edema, cyanosis, orthodeoxia-platypnea, and paradoxical embolism. Transcatheter closure of the ASD is currently available for secundum type of ASDs, and currently, there are two FDA-approved devices in the United States for the closure of ASD (see Image. Atrial Septal Defect Closure). | Catheter Management of Atrial Septal Defect -- Introduction. Atrial septal defect (ASD) is one of the most common congenital heart defects with an estimated incidence of 6 to 10 per 10,000 live births. [1] Atrial septal defects are classified as primum, secundum, sinus venosus, and coronary sinus defects. The onset of symptoms varies among different patients, and many patients remain asymptomatic. Larger defects tend to cause symptoms early on, and smaller defects cause symptoms later in life. Symptoms include failure to thrive, shortness of breath, palpitations, enlargement of right heart chambers, peripheral edema, cyanosis, orthodeoxia-platypnea, and paradoxical embolism. Transcatheter closure of the ASD is currently available for secundum type of ASDs, and currently, there are two FDA-approved devices in the United States for the closure of ASD (see Image. Atrial Septal Defect Closure). |
article-51306_3 | Catheter Management of Atrial Septal Defect -- Anatomy and Physiology | The heart comprises four chambers; the two upper chambers are referred to as the atria, and the two lower chambers are referred to as the ventricles. The inter-atrial septum divides the atrium into the right and the left atria. Similarly, a septum separates the ventricles into the right and left and is called the inter-ventricular septum. Embryologically the inter-atrial septum is derived from the septum primum and the septum secundum. The septum primum arises from the roof of the atrium and develops towards the endocardial cushions covering the ostium primum. This is followed by degeneration of the septum primum towards the roof of the atria creating the ostium secundum. Next, the septum secundum arises from the atrial roof on the right atrial side and grows caudally to cover the ostium secundum. [2] Depending on the location of the defect, ASDs are classified into primum, secundum, sinus venosus, and coronary sinus defects. Defects of the inter-atrial septum at the ostium secundum (fossa ovalis) are referred to as secundum type ASD, which is the most common type of ASD. The primum defects involve the ostium primum and the endocardial cushions and are associated with atrioventricular valvular abnormalities. The sinus venosus defects are located at the junction of the superior or inferior vena cava with the right atrium and are called superior and inferior sinus venosus defects in relation to the superior or inferior vena cava. The superior sinus venosus defects are associated with anomalous pulmonary vein connections. In the coronary sinus defect, there is a loss of the roof of the coronary sinus that allows for direct communication between the left atrium and the coronary sinus. [3] Based on the size, ASDs are classified into [4] : | Catheter Management of Atrial Septal Defect -- Anatomy and Physiology. The heart comprises four chambers; the two upper chambers are referred to as the atria, and the two lower chambers are referred to as the ventricles. The inter-atrial septum divides the atrium into the right and the left atria. Similarly, a septum separates the ventricles into the right and left and is called the inter-ventricular septum. Embryologically the inter-atrial septum is derived from the septum primum and the septum secundum. The septum primum arises from the roof of the atrium and develops towards the endocardial cushions covering the ostium primum. This is followed by degeneration of the septum primum towards the roof of the atria creating the ostium secundum. Next, the septum secundum arises from the atrial roof on the right atrial side and grows caudally to cover the ostium secundum. [2] Depending on the location of the defect, ASDs are classified into primum, secundum, sinus venosus, and coronary sinus defects. Defects of the inter-atrial septum at the ostium secundum (fossa ovalis) are referred to as secundum type ASD, which is the most common type of ASD. The primum defects involve the ostium primum and the endocardial cushions and are associated with atrioventricular valvular abnormalities. The sinus venosus defects are located at the junction of the superior or inferior vena cava with the right atrium and are called superior and inferior sinus venosus defects in relation to the superior or inferior vena cava. The superior sinus venosus defects are associated with anomalous pulmonary vein connections. In the coronary sinus defect, there is a loss of the roof of the coronary sinus that allows for direct communication between the left atrium and the coronary sinus. [3] Based on the size, ASDs are classified into [4] : |
article-51306_4 | Catheter Management of Atrial Septal Defect -- Anatomy and Physiology | Trivial: Less than 3 mm in diameter Small: 3 to less than 6 mm in diameter Moderate: 6 to 8 mm in diameter Large: Greater than 8 mm in diameter [4] | Catheter Management of Atrial Septal Defect -- Anatomy and Physiology. Trivial: Less than 3 mm in diameter Small: 3 to less than 6 mm in diameter Moderate: 6 to 8 mm in diameter Large: Greater than 8 mm in diameter [4] |
article-51306_5 | Catheter Management of Atrial Septal Defect -- Indications | Transcatheter closure of the ASD can be performed for only the secundum type of ASDs. The other ASD types are repaired surgically because of their location and associated abnormalities of atrioventricular valve defects (primum type) and anomalous pulmonary vein connections (sinus venosus type). Current indications for ASD closure by a transcatheter approach include: Symptomatic ASD causing functional impairment (Class I) Symptomatic (Class I) or asymptomatic right atrial and or right ventricular enlargement (Class II) Symptomatic (Class I) of the asymptomatic hemodynamically significant defect without symptoms (Ratio of pulmonary to systemic flow greater than 1.5) (class II) Paradoxical embolism [5] [6] [7] | Catheter Management of Atrial Septal Defect -- Indications. Transcatheter closure of the ASD can be performed for only the secundum type of ASDs. The other ASD types are repaired surgically because of their location and associated abnormalities of atrioventricular valve defects (primum type) and anomalous pulmonary vein connections (sinus venosus type). Current indications for ASD closure by a transcatheter approach include: Symptomatic ASD causing functional impairment (Class I) Symptomatic (Class I) or asymptomatic right atrial and or right ventricular enlargement (Class II) Symptomatic (Class I) of the asymptomatic hemodynamically significant defect without symptoms (Ratio of pulmonary to systemic flow greater than 1.5) (class II) Paradoxical embolism [5] [6] [7] |
article-51306_6 | Catheter Management of Atrial Septal Defect -- Contraindications | Contraindications for ASD closure by a transcatheter approach include: ASDs other than those of the secundum type, including primum type, sinus venosus type, and coronary sinus defects Severe pulmonary hypertension (pulmonary systolic pressure or pulmonary vascular resistance greater than two-thirds of systemic pressure or systemic vascular resistance) Eisenmenger syndrome or net right to left shunt Defects larger than 38 mm in diameter Absent or insufficient rim of tissue around the defect [5] [7] | Catheter Management of Atrial Septal Defect -- Contraindications. Contraindications for ASD closure by a transcatheter approach include: ASDs other than those of the secundum type, including primum type, sinus venosus type, and coronary sinus defects Severe pulmonary hypertension (pulmonary systolic pressure or pulmonary vascular resistance greater than two-thirds of systemic pressure or systemic vascular resistance) Eisenmenger syndrome or net right to left shunt Defects larger than 38 mm in diameter Absent or insufficient rim of tissue around the defect [5] [7] |
article-51306_7 | Catheter Management of Atrial Septal Defect -- Equipment | Cardiac catheterization laboratory Transesophageal echocardiography (TEE) or intracardiac echocardiogram (ICE) ASD closure device Catheter delivery system Fluoroscopy Anesthesia Antibiotics [8] | Catheter Management of Atrial Septal Defect -- Equipment. Cardiac catheterization laboratory Transesophageal echocardiography (TEE) or intracardiac echocardiogram (ICE) ASD closure device Catheter delivery system Fluoroscopy Anesthesia Antibiotics [8] |
article-51306_8 | Catheter Management of Atrial Septal Defect -- Personnel | Interventional cardiologist trained and experienced in structural heart disease, cardiovascular cath laboratory nurse, first assistant, and cardiac cath laboratory technician. | Catheter Management of Atrial Septal Defect -- Personnel. Interventional cardiologist trained and experienced in structural heart disease, cardiovascular cath laboratory nurse, first assistant, and cardiac cath laboratory technician. |
article-51306_9 | Catheter Management of Atrial Septal Defect -- Preparation -- Pre-Procedure Evaluation | The patient should be evaluated clinically and through history, including any allergies should be assessed especially to metals such as nickel. The patient should undergo a transesophageal echocardiogram to evaluate the type of ASD and its suitability for repair, such as assessing the rims of tissue around the ASD. The defect size should be measured to size the device. The patient should also undergo a right heart catheterization to assess the pulmonary pressures and the shunt fraction. Cardiac magnetic resonance imaging or cardiac CT angiography is recommended to assess the defect and anomalous pulmonary vein connections if this cannot be assessed during the transesophageal echocardiogram. | Catheter Management of Atrial Septal Defect -- Preparation -- Pre-Procedure Evaluation. The patient should be evaluated clinically and through history, including any allergies should be assessed especially to metals such as nickel. The patient should undergo a transesophageal echocardiogram to evaluate the type of ASD and its suitability for repair, such as assessing the rims of tissue around the ASD. The defect size should be measured to size the device. The patient should also undergo a right heart catheterization to assess the pulmonary pressures and the shunt fraction. Cardiac magnetic resonance imaging or cardiac CT angiography is recommended to assess the defect and anomalous pulmonary vein connections if this cannot be assessed during the transesophageal echocardiogram. |
article-51306_10 | Catheter Management of Atrial Septal Defect -- Preparation -- Pre-Procedure Evaluation | Once eligibility is determined, the patient should be counseled about the risks and benefits of undergoing the procedure, and consent should be obtained. On the day of the procedure, the patient should be evaluated for any active ongoing infections and determine suitability for anesthesia. | Catheter Management of Atrial Septal Defect -- Preparation -- Pre-Procedure Evaluation. Once eligibility is determined, the patient should be counseled about the risks and benefits of undergoing the procedure, and consent should be obtained. On the day of the procedure, the patient should be evaluated for any active ongoing infections and determine suitability for anesthesia. |
article-51306_11 | Catheter Management of Atrial Septal Defect -- Technique or Treatment | Transcatheter closure of ASD is performed under moderate sedation or general anesthesia depending on the complexity of the defect and the need for TEE imaging. But the vast majority of the ASD defects can be closed under moderate sedation. A preoperative antibiotic is administered before the procedure. After sedating the patient, vascular access is obtained in the femoral vein. Depending on the operator's preference, venous access can be obtained on the right femoral vein, or bilateral femoral veins can be used. Two accesses are required to perform the procedure if using ICE for imaging. If TEE is used, then a single venous access is adequate. Access for the ICE catheter requires an 8-10 French sheath placement and preferably a length of 25-35 cm sheaths are used as this gives stability to the ICE catheter and helps avoid the tortuosity of the femoral veins. The second access, depending on the operator preference, can start with a 6 French and can be upgraded to the appropriate sheath size in the range of 6-12 French depending on the size of the closure device being used. The higher size sheaths are required for delivering larger sized devices. Additional arterial access may be obtained for pressure monitoring, depending on the operator. Once both accesses are obtained, the patient is anticoagulated, preferably with unfractionated heparin, but other agents such as bivalirudin can be used for patients with heparin allergy. ACT of > 250 is maintained for the duration of the procedure. | Catheter Management of Atrial Septal Defect -- Technique or Treatment. Transcatheter closure of ASD is performed under moderate sedation or general anesthesia depending on the complexity of the defect and the need for TEE imaging. But the vast majority of the ASD defects can be closed under moderate sedation. A preoperative antibiotic is administered before the procedure. After sedating the patient, vascular access is obtained in the femoral vein. Depending on the operator's preference, venous access can be obtained on the right femoral vein, or bilateral femoral veins can be used. Two accesses are required to perform the procedure if using ICE for imaging. If TEE is used, then a single venous access is adequate. Access for the ICE catheter requires an 8-10 French sheath placement and preferably a length of 25-35 cm sheaths are used as this gives stability to the ICE catheter and helps avoid the tortuosity of the femoral veins. The second access, depending on the operator preference, can start with a 6 French and can be upgraded to the appropriate sheath size in the range of 6-12 French depending on the size of the closure device being used. The higher size sheaths are required for delivering larger sized devices. Additional arterial access may be obtained for pressure monitoring, depending on the operator. Once both accesses are obtained, the patient is anticoagulated, preferably with unfractionated heparin, but other agents such as bivalirudin can be used for patients with heparin allergy. ACT of > 250 is maintained for the duration of the procedure. |
article-51306_12 | Catheter Management of Atrial Septal Defect -- Technique or Treatment | Next, the ICE catheter is advanced under fluoroscopic guidance into the right atrium and positioned to visualize the interatrial septum. Thereafter the septum is then visualized, and the interatrial septum is interrogated for the presence of appropriate rim size. The ASD size is measured in multiple planes, and color flow and the direction of the shunt are recorded. After this, an angled tip catheter is advanced over a J-tip guidewire into the right atrium. The defect is crossed with the J-tip guidewire from the right atrium into the left atrium under fluoroscopic and ICE guidance. Thereafter the J-tip guidewire is advanced into the left superior pulmonary vein, and the catheter is advanced into the left superior pulmonary vein. The J-tip guidewire is then exchanged for a super stiff guidewire, and the angled tip catheter is removed. After this, the venous sheath in the femoral vein is removed, and an ASD sizing balloon is advanced over the wire into the ASD. Under fluoroscopic guidance, the sizing balloon is slowly inflated with contrast until the flow across the ASD stops as visualized by the ICE. At this, care should be taken to avoid overinflation of the balloon as this will overestimate the size of the defect. The preferable approach is to deflate the balloon until the flow across the ASD resumes and thereafter inflate the balloon until the flow across the ASD ceases again; this is called the "stop-flow" technique. Next, the size of the defect will be measured on both fluoroscopy and the ICE using the indentation marks on the ASD sizing balloon. After this, the balloon is deflated and removed over the wire with care taken to prevent the wire from prolapsing out from the pulmonary vein. Following this, the appropriately sized sheath that can deliver the ASD device is advanced over the wire into the left atrium, and the sheath dilator and the wire are removed. A stopcock or a syringe should be attached to the sheath to prevent inadvertent air entry into the sheath. | Catheter Management of Atrial Septal Defect -- Technique or Treatment. Next, the ICE catheter is advanced under fluoroscopic guidance into the right atrium and positioned to visualize the interatrial septum. Thereafter the septum is then visualized, and the interatrial septum is interrogated for the presence of appropriate rim size. The ASD size is measured in multiple planes, and color flow and the direction of the shunt are recorded. After this, an angled tip catheter is advanced over a J-tip guidewire into the right atrium. The defect is crossed with the J-tip guidewire from the right atrium into the left atrium under fluoroscopic and ICE guidance. Thereafter the J-tip guidewire is advanced into the left superior pulmonary vein, and the catheter is advanced into the left superior pulmonary vein. The J-tip guidewire is then exchanged for a super stiff guidewire, and the angled tip catheter is removed. After this, the venous sheath in the femoral vein is removed, and an ASD sizing balloon is advanced over the wire into the ASD. Under fluoroscopic guidance, the sizing balloon is slowly inflated with contrast until the flow across the ASD stops as visualized by the ICE. At this, care should be taken to avoid overinflation of the balloon as this will overestimate the size of the defect. The preferable approach is to deflate the balloon until the flow across the ASD resumes and thereafter inflate the balloon until the flow across the ASD ceases again; this is called the "stop-flow" technique. Next, the size of the defect will be measured on both fluoroscopy and the ICE using the indentation marks on the ASD sizing balloon. After this, the balloon is deflated and removed over the wire with care taken to prevent the wire from prolapsing out from the pulmonary vein. Following this, the appropriately sized sheath that can deliver the ASD device is advanced over the wire into the left atrium, and the sheath dilator and the wire are removed. A stopcock or a syringe should be attached to the sheath to prevent inadvertent air entry into the sheath. |
article-51306_13 | Catheter Management of Atrial Septal Defect -- Technique or Treatment | Next, the appropriately sized ASD device is prepped. The device is first checked for integrity, and the device is immersed in a saline tub. After this, the device is attached to the delivery cable, and the device is slowly pulled back into the loader sheath while the side flush of the loader sheath is constantly flushed to prevent any air from being trapped in the device or the loader sheath. Next, the loader is attached to the delivery sheath carefully without the introduction of air. The delivery cable is advanced into the sheath, thereby advancing the device into the delivery sheath. Thereafter, the device is slowly advanced towards the tip of the sheath under fluoroscopic guidance. At this point, care should be taken to reposition the ICE catheter to optimize the visualization of the ASD as sometimes the ICE catheter moves while the above steps are being performed. Once the device reaches the tip of the sheath, then the sheath is withdrawn over the delivery cable to unsheath the left atrial disc. This can be visualized on both ICE and fluoroscopy. Once the left atrial disc is fully formed, both the delivery sheath and the delivery cable are withdrawn until the left atrial disc is well apposed to the interatrial septum on the left atrial side. A little tension should be maintained to cause tenting of the interatrial septum. Excess tension on the sheath or the delivery cable during this step may cause the left atrial disc to prolapse into the right atrium, in which case the left atrial disc should be withdrawn into the sheath. The device should be removed, and the entire steps from crossing the septum to the advancement of the sheath should be repeated. | Catheter Management of Atrial Septal Defect -- Technique or Treatment. Next, the appropriately sized ASD device is prepped. The device is first checked for integrity, and the device is immersed in a saline tub. After this, the device is attached to the delivery cable, and the device is slowly pulled back into the loader sheath while the side flush of the loader sheath is constantly flushed to prevent any air from being trapped in the device or the loader sheath. Next, the loader is attached to the delivery sheath carefully without the introduction of air. The delivery cable is advanced into the sheath, thereby advancing the device into the delivery sheath. Thereafter, the device is slowly advanced towards the tip of the sheath under fluoroscopic guidance. At this point, care should be taken to reposition the ICE catheter to optimize the visualization of the ASD as sometimes the ICE catheter moves while the above steps are being performed. Once the device reaches the tip of the sheath, then the sheath is withdrawn over the delivery cable to unsheath the left atrial disc. This can be visualized on both ICE and fluoroscopy. Once the left atrial disc is fully formed, both the delivery sheath and the delivery cable are withdrawn until the left atrial disc is well apposed to the interatrial septum on the left atrial side. A little tension should be maintained to cause tenting of the interatrial septum. Excess tension on the sheath or the delivery cable during this step may cause the left atrial disc to prolapse into the right atrium, in which case the left atrial disc should be withdrawn into the sheath. The device should be removed, and the entire steps from crossing the septum to the advancement of the sheath should be repeated. |
article-51306_14 | Catheter Management of Atrial Septal Defect -- Technique or Treatment | Once the left atrial disc anchors well on the left side of the septum and there are sufficient tension on the interatrial septum by the left atrial disc, the next step would be to unsheath the right atrial disc carefully. After this, the sheath is slightly withdrawn away from the right atrial disc to decrease tension on the device. After this, ICE is used to examine the stability of the device, and color doppler imaging is performed to verify that the ASD is well sealed. Color flow may be noted across the waist and the center of the device, but color flow at the edges of the discs or away from the disc suggests that the device may be smaller in size, or there may be additional ASD's away from the current ASD location. In either case, the device should be captured back into the sheath, and the septum examined again for the presence of other ASD's in proximity. In this situation, the device can be upgraded to a bigger sized ASD device or cribriform occluder if the other ASD's are close to the primary ASD. If the other ASD's are > 7 mm from the primary ASD, then the other defects need to be closed using additional ASD occluders. If there is no color flow across the device, then the delivery cable is wiggled with a strong push and pull (Minnesota Wiggle) to examine the stability of the device by both fluoroscopy and ICE. If the device looks stable and there is no flow across the device, the device is released. Once the device is released, the stability and color flow are again checked, and if they are satisfactory, then the sheath is withdrawn into the inferior vena cava. Following this, the ICE imaging is performed to visualize the device and look for pericardial effusion. If everything looks satisfactory, then the ICE catheter is withdrawn from the body. Next, both the femoral venous sheath and the delivery sheath are withdrawn from the body, and either a figure of 8 stitch is placed, or manual pressure is held to achieve hemostasis. Protamine may be given to reverse the anticoagulation at this time, depending on operator preference. | Catheter Management of Atrial Septal Defect -- Technique or Treatment. Once the left atrial disc anchors well on the left side of the septum and there are sufficient tension on the interatrial septum by the left atrial disc, the next step would be to unsheath the right atrial disc carefully. After this, the sheath is slightly withdrawn away from the right atrial disc to decrease tension on the device. After this, ICE is used to examine the stability of the device, and color doppler imaging is performed to verify that the ASD is well sealed. Color flow may be noted across the waist and the center of the device, but color flow at the edges of the discs or away from the disc suggests that the device may be smaller in size, or there may be additional ASD's away from the current ASD location. In either case, the device should be captured back into the sheath, and the septum examined again for the presence of other ASD's in proximity. In this situation, the device can be upgraded to a bigger sized ASD device or cribriform occluder if the other ASD's are close to the primary ASD. If the other ASD's are > 7 mm from the primary ASD, then the other defects need to be closed using additional ASD occluders. If there is no color flow across the device, then the delivery cable is wiggled with a strong push and pull (Minnesota Wiggle) to examine the stability of the device by both fluoroscopy and ICE. If the device looks stable and there is no flow across the device, the device is released. Once the device is released, the stability and color flow are again checked, and if they are satisfactory, then the sheath is withdrawn into the inferior vena cava. Following this, the ICE imaging is performed to visualize the device and look for pericardial effusion. If everything looks satisfactory, then the ICE catheter is withdrawn from the body. Next, both the femoral venous sheath and the delivery sheath are withdrawn from the body, and either a figure of 8 stitch is placed, or manual pressure is held to achieve hemostasis. Protamine may be given to reverse the anticoagulation at this time, depending on operator preference. |
article-51306_15 | Catheter Management of Atrial Septal Defect -- Technique or Treatment | The patient is given clopidogrel 300-600 mg orally in addition to aspirin, and dual antiplatelet therapy is continued for 6 months after the procedure. After the procedure, the patient is monitored overnight. A follow-up echocardiogram is performed the following day to verify the stability of the device and rule out any erosion from the device and rule out any pericardial effusion. If everything is satisfactory, then the patient is discharged, and the patient is followed up in 6 months with a repeat echocardiogram. Infective endocarditis prophylaxis is recommended for 6 months for dental procedures. [9] [10] | Catheter Management of Atrial Septal Defect -- Technique or Treatment. The patient is given clopidogrel 300-600 mg orally in addition to aspirin, and dual antiplatelet therapy is continued for 6 months after the procedure. After the procedure, the patient is monitored overnight. A follow-up echocardiogram is performed the following day to verify the stability of the device and rule out any erosion from the device and rule out any pericardial effusion. If everything is satisfactory, then the patient is discharged, and the patient is followed up in 6 months with a repeat echocardiogram. Infective endocarditis prophylaxis is recommended for 6 months for dental procedures. [9] [10] |
article-51306_16 | Catheter Management of Atrial Septal Defect -- Complications | Major complications related to the transcatheter ASD closure include: Device embolization Erosion of the cardiac structures from the device Atrial arrhythmias Atrioventricular block (AV block) Persistent atrial aneurysm Thromboembolism Pericardial effusion and tamponade [11] [12] [13] | Catheter Management of Atrial Septal Defect -- Complications. Major complications related to the transcatheter ASD closure include: Device embolization Erosion of the cardiac structures from the device Atrial arrhythmias Atrioventricular block (AV block) Persistent atrial aneurysm Thromboembolism Pericardial effusion and tamponade [11] [12] [13] |
article-51306_17 | Catheter Management of Atrial Septal Defect -- Clinical Significance | Current guidelines recommend either surgery or transcatheter closure of the secundum ASD. However, transcatheter closure of the ASD is a relatively safe and effective procedure for the closure of the ASD in appropriately selected patients and is associated with low morbidity. Therefore, transcatheter closure has become the choice of therapy for the closure of secundum ASD defects. | Catheter Management of Atrial Septal Defect -- Clinical Significance. Current guidelines recommend either surgery or transcatheter closure of the secundum ASD. However, transcatheter closure of the ASD is a relatively safe and effective procedure for the closure of the ASD in appropriately selected patients and is associated with low morbidity. Therefore, transcatheter closure has become the choice of therapy for the closure of secundum ASD defects. |
article-51306_18 | Catheter Management of Atrial Septal Defect -- Enhancing Healthcare Team Outcomes | Transcatheter ASD closure is a relatively safe procedure with a low complication rate and faster recovery. An interprofessional heart team approach is recommended for a thorough evaluation of the patient by a cardiologist and an interventional cardiologist experienced in treating structural heart disease to assess the appropriate treatment strategy for every patient. Typically, these procedures should be performed at high-volume centers to obtain optimal outcomes. | Catheter Management of Atrial Septal Defect -- Enhancing Healthcare Team Outcomes. Transcatheter ASD closure is a relatively safe procedure with a low complication rate and faster recovery. An interprofessional heart team approach is recommended for a thorough evaluation of the patient by a cardiologist and an interventional cardiologist experienced in treating structural heart disease to assess the appropriate treatment strategy for every patient. Typically, these procedures should be performed at high-volume centers to obtain optimal outcomes. |
article-51306_19 | Catheter Management of Atrial Septal Defect -- Review Questions | Access free multiple choice questions on this topic. Comment on this article. | Catheter Management of Atrial Septal Defect -- Review Questions. Access free multiple choice questions on this topic. Comment on this article. |
article-28498_0 | Reverse Transcriptase Inhibitors -- Continuing Education Activity | Reverse transcriptase inhibitors are medications used in the management and treatment of HIV. It is in the antiretroviral class of drugs. This activity reviews the indication, action, and contraindications for RTIs as a valuable agent in managing HIV (and other disorders when applicable). This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the interprofessional healthcare team in the (management of patients with HIV and related conditions. | Reverse Transcriptase Inhibitors -- Continuing Education Activity. Reverse transcriptase inhibitors are medications used in the management and treatment of HIV. It is in the antiretroviral class of drugs. This activity reviews the indication, action, and contraindications for RTIs as a valuable agent in managing HIV (and other disorders when applicable). This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the interprofessional healthcare team in the (management of patients with HIV and related conditions. |
article-28498_1 | Reverse Transcriptase Inhibitors -- Continuing Education Activity | Objectives: Identify the mechanism of action of reverse transcriptase inhibitors. Describe the potential adverse effects when patients receive reverse transcriptase inhibitors. Review appropriate monitoring during therapy with reverse transcriptase inhibitors. Summarize interprofessional team strategies for improving care coordination and communication to advance reverse transcriptase inhibitor use and improve outcomes. Access free multiple choice questions on this topic. | Reverse Transcriptase Inhibitors -- Continuing Education Activity. Objectives: Identify the mechanism of action of reverse transcriptase inhibitors. Describe the potential adverse effects when patients receive reverse transcriptase inhibitors. Review appropriate monitoring during therapy with reverse transcriptase inhibitors. Summarize interprofessional team strategies for improving care coordination and communication to advance reverse transcriptase inhibitor use and improve outcomes. Access free multiple choice questions on this topic. |
article-28498_2 | Reverse Transcriptase Inhibitors -- Indications | With the rise of the HIV/AIDS epidemic, numerous companies have created medications to hopefully decrease the spread and potentially cure this problem. At the forefront of these medications are the reverse transcriptase inhibitors. To date, the FDA has approved the use of reverse transcriptase inhibitors for two main viral infections. The first approved use is for the treatment of HIV, specifically the HIV-1 strain. The second virus is hepatitis B. [1] Reverse transcriptase inhibitors have also been used for post-exposure prophylaxis when concern exists for potential patient infection with HIV. Lastly, reverse transcriptase inhibitors are being used to decrease the spread of HIV from mother to child during pregnancy and labor and delivery. [2] The drug of choice for HIV treatment of the mother during pregnancy is zidovudine-based antiretroviral therapy. | Reverse Transcriptase Inhibitors -- Indications. With the rise of the HIV/AIDS epidemic, numerous companies have created medications to hopefully decrease the spread and potentially cure this problem. At the forefront of these medications are the reverse transcriptase inhibitors. To date, the FDA has approved the use of reverse transcriptase inhibitors for two main viral infections. The first approved use is for the treatment of HIV, specifically the HIV-1 strain. The second virus is hepatitis B. [1] Reverse transcriptase inhibitors have also been used for post-exposure prophylaxis when concern exists for potential patient infection with HIV. Lastly, reverse transcriptase inhibitors are being used to decrease the spread of HIV from mother to child during pregnancy and labor and delivery. [2] The drug of choice for HIV treatment of the mother during pregnancy is zidovudine-based antiretroviral therapy. |
article-28498_3 | Reverse Transcriptase Inhibitors -- Indications | Research and trials are currently underway to assess the efficacy of reverse transcriptase inhibitors for pre-exposure prophylaxis. Studies show that there is anywhere from a 67% to 75% reduction in the risk of becoming infected by using pre-exposure prophylaxis. [3] While the results have been promising, some have raised strong concerns for the emergence of drug-resistant strains due to a lack of adherence to pre-exposure prophylaxis protocol by patients. The most significant factor in the success of these therapies has been the lack of adherence to the protocol by patients. [2] | Reverse Transcriptase Inhibitors -- Indications. Research and trials are currently underway to assess the efficacy of reverse transcriptase inhibitors for pre-exposure prophylaxis. Studies show that there is anywhere from a 67% to 75% reduction in the risk of becoming infected by using pre-exposure prophylaxis. [3] While the results have been promising, some have raised strong concerns for the emergence of drug-resistant strains due to a lack of adherence to pre-exposure prophylaxis protocol by patients. The most significant factor in the success of these therapies has been the lack of adherence to the protocol by patients. [2] |
article-28498_4 | Reverse Transcriptase Inhibitors -- Mechanism of Action | Within the class of reverse transcriptase inhibitors are two subclasses of drugs. The first class is the nucleoside/nucleotide reverse transcriptase inhibitors, and the second class is the non-nucleoside reverse transcriptase inhibitors. | Reverse Transcriptase Inhibitors -- Mechanism of Action. Within the class of reverse transcriptase inhibitors are two subclasses of drugs. The first class is the nucleoside/nucleotide reverse transcriptase inhibitors, and the second class is the non-nucleoside reverse transcriptase inhibitors. |
article-28498_5 | Reverse Transcriptase Inhibitors -- Mechanism of Action | The nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) were the first class of antiretroviral drugs to be approved by the FDA. NRTIs are taken as prodrugs and must be taken into the host cell and phosphorylated before they become active. Once inside the host cell, cellular kinases will activate the drug. The drug exerts its effect through its structure. NRTIs lack a 3’-hydroxyl group at the 2’-deoxyribosyl moiety and will have either a nucleoside or nucleotide as a base. Due to the missing 3’hydroxyl group, the NRTI prevents the formation of a 3’-5’-phosphodiester bond in growing DNA chains and can prevent replication of the virus. An interesting feature of these drugs is that their incorporation during RNA-dependent DNA or DNA-dependent DNA synthesis, which inhibits the production of either positive or negative strands of the DNA. | Reverse Transcriptase Inhibitors -- Mechanism of Action. The nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) were the first class of antiretroviral drugs to be approved by the FDA. NRTIs are taken as prodrugs and must be taken into the host cell and phosphorylated before they become active. Once inside the host cell, cellular kinases will activate the drug. The drug exerts its effect through its structure. NRTIs lack a 3’-hydroxyl group at the 2’-deoxyribosyl moiety and will have either a nucleoside or nucleotide as a base. Due to the missing 3’hydroxyl group, the NRTI prevents the formation of a 3’-5’-phosphodiester bond in growing DNA chains and can prevent replication of the virus. An interesting feature of these drugs is that their incorporation during RNA-dependent DNA or DNA-dependent DNA synthesis, which inhibits the production of either positive or negative strands of the DNA. |
article-28498_6 | Reverse Transcriptase Inhibitors -- Mechanism of Action | Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are the second class of reverse transcriptase inhibitors. The primary mechanism of action is through the binding of the NNRTI to the reverse transcriptase and the creation of a hydrophobic pocket proximal to the active site. This pocket creates a new spatial configuration of the substrate-binding site to reduce the overall polymerase activity. By creating a different configuration, DNA synthesis becomes slowed overall. Because of the non-competitive inhibitor action of NNRTI, it is not effective against HIV-2 reverse transcriptase. [4] | Reverse Transcriptase Inhibitors -- Mechanism of Action. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are the second class of reverse transcriptase inhibitors. The primary mechanism of action is through the binding of the NNRTI to the reverse transcriptase and the creation of a hydrophobic pocket proximal to the active site. This pocket creates a new spatial configuration of the substrate-binding site to reduce the overall polymerase activity. By creating a different configuration, DNA synthesis becomes slowed overall. Because of the non-competitive inhibitor action of NNRTI, it is not effective against HIV-2 reverse transcriptase. [4] |
article-28498_7 | Reverse Transcriptase Inhibitors -- Administration | Standard of care for HIV treatment requires the combination of NRTI, NNRTI, protease inhibitors, and integrase strand transfer inhibitors. Currently, the recommended regimen consists of a "2+1" method where the patient should start on 2 NRTIs followed by either an NNRTI, a protease inhibitor (with ritonavir boosting), or an integrase inhibitor. As for selecting the NRTI, a variety of factors like HIV strain sensitivity, contraindications, adverse reactions, and current medications should be taken into account. The International Antiretroviral Society recommends that treatment starts on the day of diagnosis to have maximum efficacy and slow the progression of the disease as quickly as possible. According to the IAS, for new HIV infections, the recommended initial treatments are integrase inhibitor-based: Dolutegravir + tenofovir alafenamide + emtricitabine Bictegravir + tenofovir alafenamide + emtricitabine For cases of preexposure prophylaxis, the recommended treatment regimen: | Reverse Transcriptase Inhibitors -- Administration. Standard of care for HIV treatment requires the combination of NRTI, NNRTI, protease inhibitors, and integrase strand transfer inhibitors. Currently, the recommended regimen consists of a "2+1" method where the patient should start on 2 NRTIs followed by either an NNRTI, a protease inhibitor (with ritonavir boosting), or an integrase inhibitor. As for selecting the NRTI, a variety of factors like HIV strain sensitivity, contraindications, adverse reactions, and current medications should be taken into account. The International Antiretroviral Society recommends that treatment starts on the day of diagnosis to have maximum efficacy and slow the progression of the disease as quickly as possible. According to the IAS, for new HIV infections, the recommended initial treatments are integrase inhibitor-based: Dolutegravir + tenofovir alafenamide + emtricitabine Bictegravir + tenofovir alafenamide + emtricitabine For cases of preexposure prophylaxis, the recommended treatment regimen: |
article-28498_8 | Reverse Transcriptase Inhibitors -- Administration | Tenofovir disoproxil fumarate + emtricitabine. Postexposure prophylaxis is attainable through either one of the following regimens for four weeks: Dolutegravir + tenofovir disoproxil fumarate + emtricitabine (preferred) Raltegravir + tenofovir disoproxil fumarate + emtricitabine | Reverse Transcriptase Inhibitors -- Administration. Tenofovir disoproxil fumarate + emtricitabine. Postexposure prophylaxis is attainable through either one of the following regimens for four weeks: Dolutegravir + tenofovir disoproxil fumarate + emtricitabine (preferred) Raltegravir + tenofovir disoproxil fumarate + emtricitabine |
article-28498_9 | Reverse Transcriptase Inhibitors -- Administration | The following list contains some of the approved drugs that fall in the NRTI and NNRTI categories of reverse transcriptase inhibitors and the dose ranges for each drug. All RTIs come in an oral tablet or solution form, with certain drugs coming in other formulations. | Reverse Transcriptase Inhibitors -- Administration. The following list contains some of the approved drugs that fall in the NRTI and NNRTI categories of reverse transcriptase inhibitors and the dose ranges for each drug. All RTIs come in an oral tablet or solution form, with certain drugs coming in other formulations. |
article-28498_10 | Reverse Transcriptase Inhibitors -- Administration -- Nucleoside/Nucleotide Reverse Transcriptase Inhibitors | Abacavir Solution 20 mg/1ml Tablet 300 mg 600 mg Lamivudine Solution 10 mg/1ml Tablet 150 mg 300 mg Stavudine Solution 1 mg/1ml Tablet 15 mg 20 mg 40 mg Didanosine Solution 10 mg/1ml Tablet 125 mg 250 mg 400 mg Zidovudine Tablet 100 mg 300 mg IV solution 10 mg/1ml Syrup 10 mg/1ml 50 mg/5ml Emtricitabine Solution 10 mg/1ml Tablet 200 mg Zalcitabine Tablet 0.375 mg 0.75 mg Tenofovir Tablet 150 mg 200 mg 300 mg | Reverse Transcriptase Inhibitors -- Administration -- Nucleoside/Nucleotide Reverse Transcriptase Inhibitors. Abacavir Solution 20 mg/1ml Tablet 300 mg 600 mg Lamivudine Solution 10 mg/1ml Tablet 150 mg 300 mg Stavudine Solution 1 mg/1ml Tablet 15 mg 20 mg 40 mg Didanosine Solution 10 mg/1ml Tablet 125 mg 250 mg 400 mg Zidovudine Tablet 100 mg 300 mg IV solution 10 mg/1ml Syrup 10 mg/1ml 50 mg/5ml Emtricitabine Solution 10 mg/1ml Tablet 200 mg Zalcitabine Tablet 0.375 mg 0.75 mg Tenofovir Tablet 150 mg 200 mg 300 mg |
article-28498_11 | Reverse Transcriptase Inhibitors -- Administration -- Non-nucleoside Reverse Transcriptase Inhibitors | Nevirapine Solution 50 mg/5ml Tablet 50 mg 200 mg 400 mg Efavirenz Solution 30 mg/1ml Tablet 50 mg 200 mg 600 mg Rilpivirine Tablet 25 mg Delavirdine Tablet 100 mg 200 mg Etravirine Tablet 25 mg 100 mg 200 mg | Reverse Transcriptase Inhibitors -- Administration -- Non-nucleoside Reverse Transcriptase Inhibitors. Nevirapine Solution 50 mg/5ml Tablet 50 mg 200 mg 400 mg Efavirenz Solution 30 mg/1ml Tablet 50 mg 200 mg 600 mg Rilpivirine Tablet 25 mg Delavirdine Tablet 100 mg 200 mg Etravirine Tablet 25 mg 100 mg 200 mg |
article-28498_12 | Reverse Transcriptase Inhibitors -- Adverse Effects | While overall safe drugs, RTIs have a variety of side effects that should be kept in mind when prescribing them. The majority of the adverse effects are seen in chronic uses situations rather than sudden onset and associated with each subcategory of the drug. | Reverse Transcriptase Inhibitors -- Adverse Effects. While overall safe drugs, RTIs have a variety of side effects that should be kept in mind when prescribing them. The majority of the adverse effects are seen in chronic uses situations rather than sudden onset and associated with each subcategory of the drug. |
article-28498_13 | Reverse Transcriptase Inhibitors -- Adverse Effects -- NRTI | The most common and the most significant adverse effect associated with the use of NRTIs is mitochondrial toxicity. While newer NRTIs have less occurrence of mitochondrial toxicity, they still carry some risk of causing it. Mitochondrial Toxicity due to the use of NRTIs can manifest as one of the following: myopathy, lipoatrophy, neuropathy, and lactic acidosis with or without hepatic steatosis. [5] Myopathy is most commonly associated with zidovudine and can manifest as proximal muscle tenderness and myalgias. | Reverse Transcriptase Inhibitors -- Adverse Effects -- NRTI. The most common and the most significant adverse effect associated with the use of NRTIs is mitochondrial toxicity. While newer NRTIs have less occurrence of mitochondrial toxicity, they still carry some risk of causing it. Mitochondrial Toxicity due to the use of NRTIs can manifest as one of the following: myopathy, lipoatrophy, neuropathy, and lactic acidosis with or without hepatic steatosis. [5] Myopathy is most commonly associated with zidovudine and can manifest as proximal muscle tenderness and myalgias. |
article-28498_14 | Reverse Transcriptase Inhibitors -- Adverse Effects -- NRTI | Lipoatrophy (also known as lipodystrophy) is the loss of body fat from the face and extremities. The loss of the fat from areas of the cheek, temples, and periorbital regions gives patients an emaciated appearance. While this effect strongly correlates with the use of protease inhibitors in HAART, it can also appear in association with stavudine use. NRTI-associated peripheral neuropathy is most common with chronic use of zalcitabine, didanosine, and lamivudine. [6] | Reverse Transcriptase Inhibitors -- Adverse Effects -- NRTI. Lipoatrophy (also known as lipodystrophy) is the loss of body fat from the face and extremities. The loss of the fat from areas of the cheek, temples, and periorbital regions gives patients an emaciated appearance. While this effect strongly correlates with the use of protease inhibitors in HAART, it can also appear in association with stavudine use. NRTI-associated peripheral neuropathy is most common with chronic use of zalcitabine, didanosine, and lamivudine. [6] |
article-28498_15 | Reverse Transcriptase Inhibitors -- Adverse Effects -- NRTI | Lactic acidosis most commonly occurs with the use of zidovudine, lamivudine, stavudine, and didanosine. Hepatic steatosis often occurs accompanying lactic acidosis due to decreased mitochondrial beta-oxidation of fatty acids resulting in esterified triglycerides that accumulate in the liver. [5] | Reverse Transcriptase Inhibitors -- Adverse Effects -- NRTI. Lactic acidosis most commonly occurs with the use of zidovudine, lamivudine, stavudine, and didanosine. Hepatic steatosis often occurs accompanying lactic acidosis due to decreased mitochondrial beta-oxidation of fatty acids resulting in esterified triglycerides that accumulate in the liver. [5] |
article-28498_16 | Reverse Transcriptase Inhibitors -- Adverse Effects -- NNRTI | When compared to NRTIs, NNRTIs have correlated with fewer adverse effects. As a group, all NNRTIs are known to cause rashes. The most severe of these rashes are Stevens-Johnson syndrome as well as toxic epidermal necrolysis. [7] | Reverse Transcriptase Inhibitors -- Adverse Effects -- NNRTI. When compared to NRTIs, NNRTIs have correlated with fewer adverse effects. As a group, all NNRTIs are known to cause rashes. The most severe of these rashes are Stevens-Johnson syndrome as well as toxic epidermal necrolysis. [7] |
article-28498_17 | Reverse Transcriptase Inhibitors -- Adverse Effects -- NNRTI | In addition to dermatitis complications through the use of NNRTIs, certain NNRTIs are known to cause other adverse effects. Nevirapine, in comparison, has been shown to cause significant transaminitis. [8] Efavirenz, unlike the other NNRTIs, has demonstrated CNS alterations. These CNS effects include problems with mood, insomnia, and disturbing dreams. Finally, delavirdine has been known to cause neutropenia when coadministered with zidovudine. [9] | Reverse Transcriptase Inhibitors -- Adverse Effects -- NNRTI. In addition to dermatitis complications through the use of NNRTIs, certain NNRTIs are known to cause other adverse effects. Nevirapine, in comparison, has been shown to cause significant transaminitis. [8] Efavirenz, unlike the other NNRTIs, has demonstrated CNS alterations. These CNS effects include problems with mood, insomnia, and disturbing dreams. Finally, delavirdine has been known to cause neutropenia when coadministered with zidovudine. [9] |
article-28498_18 | Reverse Transcriptase Inhibitors -- Contraindications | While reverse transcriptase inhibitors are generally safe to use, contraindications do exist to prevent severe adverse effects associated with their use. First and foremost, a prior history of hypersensitivity to RTIs is a contraindication for their use. If a patient has had an adverse reaction to one RTI, they should discontinue the drug and a different agent prescribed. | Reverse Transcriptase Inhibitors -- Contraindications. While reverse transcriptase inhibitors are generally safe to use, contraindications do exist to prevent severe adverse effects associated with their use. First and foremost, a prior history of hypersensitivity to RTIs is a contraindication for their use. If a patient has had an adverse reaction to one RTI, they should discontinue the drug and a different agent prescribed. |
article-28498_19 | Reverse Transcriptase Inhibitors -- Contraindications | Abacavir is explicitly associated with a life-threatening hypersensitivity reaction in 5% of patients. Specifically, patients carrying the HLA-B*5701 allele have the highest chance of experiencing a severe reaction to the drug. Patients with HLA-DR7 and HLA-DQ3 should also avoid the use of abacavir. [10] Patients with elevated or abnormal baseline ALT or AST should avoid the use of nevirapine-based antiretroviral therapy due to severe hepatotoxicity and rash-associated hepatotoxicity. [11] Didanosine has also demonstrated a clinically significant drug interaction when taken concomitantly with allopurinol. [12] | Reverse Transcriptase Inhibitors -- Contraindications. Abacavir is explicitly associated with a life-threatening hypersensitivity reaction in 5% of patients. Specifically, patients carrying the HLA-B*5701 allele have the highest chance of experiencing a severe reaction to the drug. Patients with HLA-DR7 and HLA-DQ3 should also avoid the use of abacavir. [10] Patients with elevated or abnormal baseline ALT or AST should avoid the use of nevirapine-based antiretroviral therapy due to severe hepatotoxicity and rash-associated hepatotoxicity. [11] Didanosine has also demonstrated a clinically significant drug interaction when taken concomitantly with allopurinol. [12] |
article-28498_20 | Reverse Transcriptase Inhibitors -- Monitoring | Monitoring for RTIs and HAART, in general, is essential due to the disastrous effects of medication noncompliance and suboptimal therapy. Monitoring mainly takes place through assessments like CD4 count and viral load. | Reverse Transcriptase Inhibitors -- Monitoring. Monitoring for RTIs and HAART, in general, is essential due to the disastrous effects of medication noncompliance and suboptimal therapy. Monitoring mainly takes place through assessments like CD4 count and viral load. |
article-28498_21 | Reverse Transcriptase Inhibitors -- Monitoring | The CD4 count is useful to measure due to this being the primary target of HIV. Patients with low CD4 counts can be expected to have severe immunodeficiencies leading to opportunistic infections. Viral load looks at how many copies of the HIV RNA are present in the patient. The greater the viral load, the greater the presence of the HIV infection. [13] | Reverse Transcriptase Inhibitors -- Monitoring. The CD4 count is useful to measure due to this being the primary target of HIV. Patients with low CD4 counts can be expected to have severe immunodeficiencies leading to opportunistic infections. Viral load looks at how many copies of the HIV RNA are present in the patient. The greater the viral load, the greater the presence of the HIV infection. [13] |
article-28498_22 | Reverse Transcriptase Inhibitors -- Monitoring | Current IAS recommendations state that patients should have an HIV RNA level (viral load) within six weeks of initiating HAART to assess adherence and tolerability of therapy while noting that proper RNA level suppression can take up to 24 weeks. Once the viral load has fallen below 50 copies/mL, the recommendation is to repeat the viral load every three months until achieving one year of suppression. After a year of successfully suppressed viral load, the patient can have their HIV RNA levels measured every six months. IAS recommends checking the CD4 cell count every six months until levels are above 250/microliter for at least one year. After achieving these goals, CD4 count measuring can cease. Unless the patient is to undergo steroid or immunosuppressive treatments, or the patient experiences HAART failure, the CD4 count does not need to be measured. The definition of HAART failure is the IAS as an HIV RNA level above 200 copies/mL on at least two consecutive measurements. After diagnosing HAART failure, the recommendation is to reassess HIV genotype and drug susceptibilities and make changes to the patient's regimen. | Reverse Transcriptase Inhibitors -- Monitoring. Current IAS recommendations state that patients should have an HIV RNA level (viral load) within six weeks of initiating HAART to assess adherence and tolerability of therapy while noting that proper RNA level suppression can take up to 24 weeks. Once the viral load has fallen below 50 copies/mL, the recommendation is to repeat the viral load every three months until achieving one year of suppression. After a year of successfully suppressed viral load, the patient can have their HIV RNA levels measured every six months. IAS recommends checking the CD4 cell count every six months until levels are above 250/microliter for at least one year. After achieving these goals, CD4 count measuring can cease. Unless the patient is to undergo steroid or immunosuppressive treatments, or the patient experiences HAART failure, the CD4 count does not need to be measured. The definition of HAART failure is the IAS as an HIV RNA level above 200 copies/mL on at least two consecutive measurements. After diagnosing HAART failure, the recommendation is to reassess HIV genotype and drug susceptibilities and make changes to the patient's regimen. |
article-28498_23 | Reverse Transcriptase Inhibitors -- Monitoring | When talking about HAART Failure, it is important to consider drug resistance as a causative agent. Drug resistance is a serious complication that must be considered and is associated with poor medication compliance. In addition, factors such as cost of treatment, accessibility to medications, and access to proper follow-up all play a significant factor in breeding resistance to standard HIV regimens. Studies have shown that low adherence and interruptions in treatment for more than two consecutive days in the first three months with NNRTI and NRTI-based regimens increased the risk of resistance within the first six months of treatment. [14] | Reverse Transcriptase Inhibitors -- Monitoring. When talking about HAART Failure, it is important to consider drug resistance as a causative agent. Drug resistance is a serious complication that must be considered and is associated with poor medication compliance. In addition, factors such as cost of treatment, accessibility to medications, and access to proper follow-up all play a significant factor in breeding resistance to standard HIV regimens. Studies have shown that low adherence and interruptions in treatment for more than two consecutive days in the first three months with NNRTI and NRTI-based regimens increased the risk of resistance within the first six months of treatment. [14] |
article-28498_24 | Reverse Transcriptase Inhibitors -- Monitoring | Studies have shown that while both measures help determine treatment efficacy, each variable offers different insights into the patient’s condition. CD4 count, when brought to a normal level through treatment, is associated with a reduced risk of mortality. When the viral load becomes undetectable, it means that the drug regimen that the patient is on is working at maximum efficacy. Also, viral load monitoring is considered a better predictor of HIV to AIDS progression than CD4 counts. [15] | Reverse Transcriptase Inhibitors -- Monitoring. Studies have shown that while both measures help determine treatment efficacy, each variable offers different insights into the patient’s condition. CD4 count, when brought to a normal level through treatment, is associated with a reduced risk of mortality. When the viral load becomes undetectable, it means that the drug regimen that the patient is on is working at maximum efficacy. Also, viral load monitoring is considered a better predictor of HIV to AIDS progression than CD4 counts. [15] |
article-28498_25 | Reverse Transcriptase Inhibitors -- Toxicity | Toxicity to RTIs mainly occurs via adverse reactions that the patient may present with (see above for a list of severe reactions). Patients should understand the serious adverse effects the drugs that make up their HAART regimen can cause. If a patient presents with an adverse effect, then the drug should be discontinued and replaced with another from the same subclass of reverse transcriptase inhibitors. Specifically for stavudine, studies suggest that switching to abacavir will help improve lipodystrophy and still maintain optimal regimen efficacy. [16] All other drugs causing adverse reactions require switching to a drug to which their specific HIV genotype is susceptible. | Reverse Transcriptase Inhibitors -- Toxicity. Toxicity to RTIs mainly occurs via adverse reactions that the patient may present with (see above for a list of severe reactions). Patients should understand the serious adverse effects the drugs that make up their HAART regimen can cause. If a patient presents with an adverse effect, then the drug should be discontinued and replaced with another from the same subclass of reverse transcriptase inhibitors. Specifically for stavudine, studies suggest that switching to abacavir will help improve lipodystrophy and still maintain optimal regimen efficacy. [16] All other drugs causing adverse reactions require switching to a drug to which their specific HIV genotype is susceptible. |
article-28498_26 | Reverse Transcriptase Inhibitors -- Enhancing Healthcare Team Outcomes | Patients on RTIs, and more importantly, HAART, should have close follow-up with the primary clinician taking care of them. Physicians should work closely with nurses to keep a proper follow-up on patients to ensure optimal therapy and look out for potential adverse effects. Physicians can also work closely with pharmacists to help optimize treatment and give the best medications to patients to achieve optimal therapy; the pharmacist can consult on the best combinations of agents and optimal dosing and administration. Nursing and pharmacy must both emphasize the importance of strict compliance to patients, as a lack of compliance can be devastating to therapy and, subsequently, their life. Concerns about compliance need to be brought to the prescribing clinician's attention immediately. All interprofessional healthcare team members are responsible for providing the best care to their patients and monitoring adverse effects. An interprofessional team will result in the best outcomes with the fewest adverse events. [Level 5] | Reverse Transcriptase Inhibitors -- Enhancing Healthcare Team Outcomes. Patients on RTIs, and more importantly, HAART, should have close follow-up with the primary clinician taking care of them. Physicians should work closely with nurses to keep a proper follow-up on patients to ensure optimal therapy and look out for potential adverse effects. Physicians can also work closely with pharmacists to help optimize treatment and give the best medications to patients to achieve optimal therapy; the pharmacist can consult on the best combinations of agents and optimal dosing and administration. Nursing and pharmacy must both emphasize the importance of strict compliance to patients, as a lack of compliance can be devastating to therapy and, subsequently, their life. Concerns about compliance need to be brought to the prescribing clinician's attention immediately. All interprofessional healthcare team members are responsible for providing the best care to their patients and monitoring adverse effects. An interprofessional team will result in the best outcomes with the fewest adverse events. [Level 5] |
article-28498_27 | Reverse Transcriptase Inhibitors -- Review Questions | Access free multiple choice questions on this topic. Comment on this article. | Reverse Transcriptase Inhibitors -- Review Questions. Access free multiple choice questions on this topic. Comment on this article. |
article-17473_0 | Amoxapine -- Continuing Education Activity | Amoxapine is classified as a second-generation tricyclic dibenzoxazepine antidepressant approved by the U.S. Food and Drug Administration (FDA). This medication is typically prescribed for managing treatment-resistant or persistent depression. Amoxapine is indicated for use in cases of depression accompanied by other psychiatric issues such as anxiety, agitation, psychosis, neurosis, or recurrent depression. The objective of this activity is to familiarize medical practitioners with the appropriate usage of amoxapine and its dosing guidelines, administration, monitoring instructions, and the adverse effects associated with this drug. This activity also highlights the critical roles of a unified interprofessional team in the treatment of patients using amoxapine for their depression. | Amoxapine -- Continuing Education Activity. Amoxapine is classified as a second-generation tricyclic dibenzoxazepine antidepressant approved by the U.S. Food and Drug Administration (FDA). This medication is typically prescribed for managing treatment-resistant or persistent depression. Amoxapine is indicated for use in cases of depression accompanied by other psychiatric issues such as anxiety, agitation, psychosis, neurosis, or recurrent depression. The objective of this activity is to familiarize medical practitioners with the appropriate usage of amoxapine and its dosing guidelines, administration, monitoring instructions, and the adverse effects associated with this drug. This activity also highlights the critical roles of a unified interprofessional team in the treatment of patients using amoxapine for their depression. |
article-17473_1 | Amoxapine -- Continuing Education Activity | Objectives: Identify appropriate patient candidates for amoxapine therapy, considering their clinical history, comorbid psychiatric conditions, and resistance to previous treatments. Differentiate amoxapine from other antidepressants, understanding its unique mechanisms of action, adverse effect profile, and potential interactions with other medications. Screen patients for contraindications, allergies, and potential risk factors associated with amoxapine use, such as seizure disorders or cardiac issues. Collaborate with other healthcare professionals, such as psychiatrists, toxicologists, and pharmacists, to ensure coordinated and comprehensive care for patients receiving amoxapine. Access free multiple choice questions on this topic. | Amoxapine -- Continuing Education Activity. Objectives: Identify appropriate patient candidates for amoxapine therapy, considering their clinical history, comorbid psychiatric conditions, and resistance to previous treatments. Differentiate amoxapine from other antidepressants, understanding its unique mechanisms of action, adverse effect profile, and potential interactions with other medications. Screen patients for contraindications, allergies, and potential risk factors associated with amoxapine use, such as seizure disorders or cardiac issues. Collaborate with other healthcare professionals, such as psychiatrists, toxicologists, and pharmacists, to ensure coordinated and comprehensive care for patients receiving amoxapine. Access free multiple choice questions on this topic. |
article-17473_2 | Amoxapine -- Indications -- FDA-Approved Indications | Amoxapine is classified as a second-generation tricyclic dibenzoxazepine antidepressant approved by the U.S. Food and Drug Administration (FDA). This medication is typically used as a second- or third-line treatment option when selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs) have failed to control depression. Thus, amoxapine is indicated for managing treatment-resistant depression when the first- and second-line medications have proven ineffective in alleviating symptoms. Amoxapine is indicated for use in cases of depression accompanied by other psychiatric issues such as anxiety, agitation, psychosis, neurosis, or recurrent depression. [1] [2] | Amoxapine -- Indications -- FDA-Approved Indications. Amoxapine is classified as a second-generation tricyclic dibenzoxazepine antidepressant approved by the U.S. Food and Drug Administration (FDA). This medication is typically used as a second- or third-line treatment option when selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs) have failed to control depression. Thus, amoxapine is indicated for managing treatment-resistant depression when the first- and second-line medications have proven ineffective in alleviating symptoms. Amoxapine is indicated for use in cases of depression accompanied by other psychiatric issues such as anxiety, agitation, psychosis, neurosis, or recurrent depression. [1] [2] |
article-17473_3 | Amoxapine -- Indications -- Off-Label Uses | Research conducted in mice has shown that amoxapine can reduce the production of amyloid-beta chains associated with Alzheimer disease by targeting the serotonin-6 (HTR-6, 5-HT-6) receptor. [3] Multiple studies have shown that amoxapine can reduce the incidence of diarrhea in patients undergoing chemotherapy, particularly when used in conjunction with irinotecan. [4] [5] Furthermore, research has highlighted amoxapine's effectiveness in the management of neuropathic pain. [6] | Amoxapine -- Indications -- Off-Label Uses. Research conducted in mice has shown that amoxapine can reduce the production of amyloid-beta chains associated with Alzheimer disease by targeting the serotonin-6 (HTR-6, 5-HT-6) receptor. [3] Multiple studies have shown that amoxapine can reduce the incidence of diarrhea in patients undergoing chemotherapy, particularly when used in conjunction with irinotecan. [4] [5] Furthermore, research has highlighted amoxapine's effectiveness in the management of neuropathic pain. [6] |
article-17473_4 | Amoxapine -- Mechanism of Action | Amoxapine, a second-generation tricyclic dibenzoxazepine antidepressant, primarily functions by inhibiting the reuptake of norepinephrine in neuronal synapses. The drug exhibits minimal effect on the histamine H1 receptor and serotonin receptors, except for the serotonin-6 receptor (HTR-6, 5-HT-6). [7] [8] [9] Furthermore, amoxapine also acts as a dopamine (DA) receptor antagonist, specifically targeting D2 and D4 receptors. [10] | Amoxapine -- Mechanism of Action. Amoxapine, a second-generation tricyclic dibenzoxazepine antidepressant, primarily functions by inhibiting the reuptake of norepinephrine in neuronal synapses. The drug exhibits minimal effect on the histamine H1 receptor and serotonin receptors, except for the serotonin-6 receptor (HTR-6, 5-HT-6). [7] [8] [9] Furthermore, amoxapine also acts as a dopamine (DA) receptor antagonist, specifically targeting D2 and D4 receptors. [10] |
article-17473_5 | Amoxapine -- Mechanism of Action -- Pharmacokinetics | Absorption: Amoxapine is rapidly absorbed in the body after oral administration. The time to peak plasma concentration for amoxapine is approximately 90 minutes. Distribution: Amoxapine exhibits a high plasma protein binding of approximately 90%. | Amoxapine -- Mechanism of Action -- Pharmacokinetics. Absorption: Amoxapine is rapidly absorbed in the body after oral administration. The time to peak plasma concentration for amoxapine is approximately 90 minutes. Distribution: Amoxapine exhibits a high plasma protein binding of approximately 90%. |
article-17473_6 | Amoxapine -- Mechanism of Action -- Pharmacokinetics | Metabolism: Amoxapine undergoes hepatic metabolism primarily via the CYP2D6 enzyme, leading to the formation of 2 active metabolites—7-hydroxy-amoxapine and 8-hydroxy-amoxapine. These active metabolites have been shown to reduce the incidence of diarrhea in patients after administering irinotecan chemotherapy. Research findings demonstrated that these metabolites effectively reduced tumor growth in patients. [5] [11] | Amoxapine -- Mechanism of Action -- Pharmacokinetics. Metabolism: Amoxapine undergoes hepatic metabolism primarily via the CYP2D6 enzyme, leading to the formation of 2 active metabolites—7-hydroxy-amoxapine and 8-hydroxy-amoxapine. These active metabolites have been shown to reduce the incidence of diarrhea in patients after administering irinotecan chemotherapy. Research findings demonstrated that these metabolites effectively reduced tumor growth in patients. [5] [11] |
article-17473_7 | Amoxapine -- Mechanism of Action -- Pharmacokinetics | Elimination: Research indicates that the active metabolite, 8-hydroxy-amoxapine, has a half-life of 30 hours, whereas the drug has a half-life of 8 hours. The primary route of drug elimination from the body is through urine, with a minor fraction excreted in the feces. [2] | Amoxapine -- Mechanism of Action -- Pharmacokinetics. Elimination: Research indicates that the active metabolite, 8-hydroxy-amoxapine, has a half-life of 30 hours, whereas the drug has a half-life of 8 hours. The primary route of drug elimination from the body is through urine, with a minor fraction excreted in the feces. [2] |
article-17473_8 | Amoxapine -- Administration -- Available Dosage Forms and Strengths | Amoxapine is available in oral tablet formulations, with strengths of 25 mg, 50 mg, 100 mg, and 150 mg doses. | Amoxapine -- Administration -- Available Dosage Forms and Strengths. Amoxapine is available in oral tablet formulations, with strengths of 25 mg, 50 mg, 100 mg, and 150 mg doses. |
article-17473_9 | Amoxapine -- Administration -- Adult Dosage | Amoxapine is typically administered orally at a starting dose of 100 mg, with the option to increase the dosage up to a maximum of 300 mg. The normal therapeutic dose for depression is between 200 and 300 mg, usually taken orally at bedtime. [12] [13] [14] Amoxapine can be administered daily to patients either as a single dose or 2 equally divided doses. [15] However, due to the prolonged half-life of the active drug metabolites, a single daily dose of amoxapine is often preferred over divided doses for more effective treatment. Antidepressant benefits from amoxapine may become noticeable within just 7 days, and more than 80% of patients experience significant improvement within 2 weeks. [7] The maximum recommended dosage of amoxapine for outpatient settings is 400 mg daily, whereas, for hospitalized patients with no history of seizures, it is 600 mg daily. | Amoxapine -- Administration -- Adult Dosage. Amoxapine is typically administered orally at a starting dose of 100 mg, with the option to increase the dosage up to a maximum of 300 mg. The normal therapeutic dose for depression is between 200 and 300 mg, usually taken orally at bedtime. [12] [13] [14] Amoxapine can be administered daily to patients either as a single dose or 2 equally divided doses. [15] However, due to the prolonged half-life of the active drug metabolites, a single daily dose of amoxapine is often preferred over divided doses for more effective treatment. Antidepressant benefits from amoxapine may become noticeable within just 7 days, and more than 80% of patients experience significant improvement within 2 weeks. [7] The maximum recommended dosage of amoxapine for outpatient settings is 400 mg daily, whereas, for hospitalized patients with no history of seizures, it is 600 mg daily. |
article-17473_10 | Amoxapine -- Administration -- Maintenance Dosage | The recommended maintenance dose for amoxapine is the minimum effective dose needed to maintain remission. If symptoms reappear, the dosage should be increased to the previous level until they are under control. Notably, it is recommended to take a single dose of ≤300 mg at bedtime for maintenance therapy. | Amoxapine -- Administration -- Maintenance Dosage. The recommended maintenance dose for amoxapine is the minimum effective dose needed to maintain remission. If symptoms reappear, the dosage should be increased to the previous level until they are under control. Notably, it is recommended to take a single dose of ≤300 mg at bedtime for maintenance therapy. |
article-17473_11 | Amoxapine -- Administration -- Specific Patient Populations | Hepatic impairment: The product labeling does not specify dosage adjustments for hepatic impairment. However, it is advisable to exercise caution when administering amoxapine to these patients, considering its liver-dependent metabolism. [11] | Amoxapine -- Administration -- Specific Patient Populations. Hepatic impairment: The product labeling does not specify dosage adjustments for hepatic impairment. However, it is advisable to exercise caution when administering amoxapine to these patients, considering its liver-dependent metabolism. [11] |
article-17473_12 | Amoxapine -- Administration -- Specific Patient Populations | Renal impairment: The product labeling does not contain specific guidance on dosage adjustments for renal impairment. Thus, it is crucial to exercise caution when prescribing amoxapine to patients with renal impairment, as its primary elimination route is through the kidneys. | Amoxapine -- Administration -- Specific Patient Populations. Renal impairment: The product labeling does not contain specific guidance on dosage adjustments for renal impairment. Thus, it is crucial to exercise caution when prescribing amoxapine to patients with renal impairment, as its primary elimination route is through the kidneys. |
article-17473_13 | Amoxapine -- Administration -- Specific Patient Populations | Pregnancy considerations: Amoxapine was previously classified by the FDA as a pregnancy category C drug. Studies on animals revealed fetotoxic effects, including intrauterine death, decreased birth weight, and stillbirth, occurring at oral doses 3 to 10 times higher than the human dose. There is limited availability of well-controlled studies involving pregnant women. Consequently, amoxapine use during pregnancy should be approached cautiously. Decisions regarding medication use in pregnant women should be made judiciously, taking into account a careful assessment of the potential benefits and risks to the fetus. [16] | Amoxapine -- Administration -- Specific Patient Populations. Pregnancy considerations: Amoxapine was previously classified by the FDA as a pregnancy category C drug. Studies on animals revealed fetotoxic effects, including intrauterine death, decreased birth weight, and stillbirth, occurring at oral doses 3 to 10 times higher than the human dose. There is limited availability of well-controlled studies involving pregnant women. Consequently, amoxapine use during pregnancy should be approached cautiously. Decisions regarding medication use in pregnant women should be made judiciously, taking into account a careful assessment of the potential benefits and risks to the fetus. [16] |
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